First, increased flux through the polyol pathway in hyperglycemic patients may lead to intracellular sorbitol accumulation and, potentially, to osmotic increase or changes in the NAD/NADH ratio induced by the flux through the aldose reductase pathway. These changes can cause direct neuronal damage or decrease neuronal blood flow, indirectly leading to peripheral nerve hypoxia.

Second, the activation of protein kinase C (PKC) in response to increased diacylglycerol levels can affect enzymes that are important for maintaining cellular membrane potential and nerve conduction. In addition, PKC activation can induce vasoconstriction and reduced neuronal blood flow.

Third, the auto-oxidation of glucose causes increased production of reactive oxygen species and the formation of advanced glycation end products (AGEs) by non-enzymatic glycation of proteins. AGEs then bind to a cell-surface receptor and cause activation of the NF-κB, which is associated with endothelial dysfunction and reduced nerve blood flow.

Fourth, diabetes impairs the hepatic Δ-6 desaturation of dietary linolenic acid to γ-linolenic acid and results in reduced synthesis of vasoactive prostanoids in the vasa nervorum. This leads to reduced blood flow and nerve  hypoxia. 

                                                                                                Aristidis Veves, George L. King, 2001

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Could it be lack of blood flow?

Of course it could!

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VasoActiv provides a patented means of increasing blood flow which not only provides a better supply of oxygen to the nerves, but also, through endothelial mechanotransduction, increases autocrine and paracrine production of critical vasoactive substances such as vasodilators, antioxidants, anti-inflammatories and anticoagulent agents. The increased flow also leads to angiogenesis and arteriogenesis for sustainable blood flow.

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PATIENT TESTIMONIALS